• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

中枢神经系统炎症中嗜中性粒细胞与星形胶质细胞的相互作用。

Neutrophils-astrocyte interactions in central nervous system inflammation.

作者信息

Yuan Bingyou, Zhang Xian, Liu Liang, Chai Yan, Zhang Jianning, Chen Xin

机构信息

Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, PR China.

Tianjin Neurological Institute, Key Laboratory of Post-Trauma Neuro-Repair and Regeneration in Central Nervous System, Ministry of Education, Tianjin, PR China.

出版信息

Cell Death Dis. 2025 Aug 25;16(1):643. doi: 10.1038/s41419-025-07945-x.

DOI:10.1038/s41419-025-07945-x
PMID:40854886
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12379155/
Abstract

The concept of central nervous system (CNS) "immune privilege" has undergone substantial revision. We now understand that the CNS exhibits sophisticated inflammatory responses that serve dual functions: potentially detrimental in acute phases while facilitating repair and recovery during chronic stages of various neurological conditions. Recent advances in genomic technologies, particularly high-throughput single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics, have revolutionized our understanding of cellular dynamics and interactions within the CNS inflammatory microenvironment. Here, we examine the intricate interplay between neutrophils and astrocytes during CNS inflammation. We synthesize emerging evidence of their reciprocal regulation, analyze their roles in neurological diseases, and delineate the molecular pathways mediating their communication. Understanding these cellular interactions could reveal promising therapeutic targets for modulating secondary CNS inflammation, potentially leading to more effective treatment strategies for neurological disorders.

摘要

中枢神经系统(CNS)“免疫特权”的概念已历经重大修订。我们现在明白,中枢神经系统会展现出复杂的炎症反应,这些反应具有双重功能:在急性期可能有害,但在各种神经疾病的慢性阶段则有助于修复和恢复。基因组技术的最新进展,尤其是高通量单细胞RNA测序(scRNA-seq)和空间转录组学,彻底改变了我们对中枢神经系统炎症微环境中细胞动态和相互作用的理解。在此,我们研究中枢神经系统炎症期间中性粒细胞与星形胶质细胞之间的复杂相互作用。我们综合了它们相互调节的新证据,分析了它们在神经疾病中的作用,并描绘了介导它们通讯的分子途径。了解这些细胞间相互作用可能会揭示出用于调节中枢神经系统继发性炎症的有前景的治疗靶点,有望为神经疾病带来更有效的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/9dbc258ac4f7/41419_2025_7945_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/d96160b539ed/41419_2025_7945_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/286312834412/41419_2025_7945_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/ea5ba0c86b1b/41419_2025_7945_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/0bb3b175c87f/41419_2025_7945_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/9dbc258ac4f7/41419_2025_7945_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/d96160b539ed/41419_2025_7945_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/286312834412/41419_2025_7945_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/ea5ba0c86b1b/41419_2025_7945_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/0bb3b175c87f/41419_2025_7945_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/978d/12379155/9dbc258ac4f7/41419_2025_7945_Fig5_HTML.jpg

相似文献

1
Neutrophils-astrocyte interactions in central nervous system inflammation.中枢神经系统炎症中嗜中性粒细胞与星形胶质细胞的相互作用。
Cell Death Dis. 2025 Aug 25;16(1):643. doi: 10.1038/s41419-025-07945-x.
2
Prescription of Controlled Substances: Benefits and Risks管制药品的处方:益处与风险
3
Lesion-remote astrocytes govern microglia-mediated white matter repair.损伤远端星形胶质细胞调控小胶质细胞介导的白质修复。
bioRxiv. 2024 Mar 17:2024.03.15.585251. doi: 10.1101/2024.03.15.585251.
4
Pathways to Progressive Disability in Multiple Sclerosis: The Role of Glial Cells in Chronic CNS Inflammation.多发性硬化症进展性残疾的途径:神经胶质细胞在慢性中枢神经系统炎症中的作用
Glia. 2025 Oct;73(10):1928-1950. doi: 10.1002/glia.70044. Epub 2025 May 23.
5
Cellular and Molecular Interactions in CNS Injury: The Role of Immune Cells and Inflammatory Responses in Damage and Repair.中枢神经系统损伤中的细胞与分子相互作用:免疫细胞及炎症反应在损伤与修复中的作用
Cells. 2025 Jun 18;14(12):918. doi: 10.3390/cells14120918.
6
TGFα controls checkpoints in CNS resident and infiltrating immune cells to promote resolution of inflammation.转化生长因子α控制中枢神经系统驻留免疫细胞和浸润免疫细胞中的检查点,以促进炎症的消退。
Nat Commun. 2025 Jun 19;16(1):5344. doi: 10.1038/s41467-025-60363-7.
7
Tissue-resident memory CD4 T cells infiltrate the CNS in progressive multiple sclerosis and contribute to chronic autoimmunity in mice.组织驻留记忆性CD4 T细胞在进展性多发性硬化症中浸润中枢神经系统,并在小鼠中导致慢性自身免疫。
Sci Transl Med. 2025 Jul 23;17(808):eadp8109. doi: 10.1126/scitranslmed.adp8109.
8
Emerging roles of astrocytes as immune effectors in the central nervous system.星形胶质细胞在中枢神经系统中作为免疫效应细胞的新作用。
Trends Immunol. 2024 Oct;45(10):824-836. doi: 10.1016/j.it.2024.08.008. Epub 2024 Sep 27.
9
Astrocytes: Therapeutic targets for stroke.星形胶质细胞:中风的治疗靶点。
Neural Regen Res. 2026 Mar 1;21(3):1074-1088. doi: 10.4103/NRR.NRR-D-24-01062. Epub 2025 Feb 24.
10
Modeling neuroinflammatory interactions between microglia and astrocytes in a human iPSC-based coculture platform.在基于人诱导多能干细胞的共培养平台中模拟小胶质细胞与星形胶质细胞之间的神经炎症相互作用。
Cell Commun Signal. 2025 Jun 20;23(1):298. doi: 10.1186/s12964-025-02304-x.

本文引用的文献

1
Skull bone marrow and skull meninges channels: redefining the landscape of central nervous system immune surveillance.颅骨骨髓和颅骨脑膜通道:重新定义中枢神经系统免疫监视格局
Cell Death Dis. 2025 Jan 29;16(1):53. doi: 10.1038/s41419-025-07336-2.
2
Osteocalcin-expressing neutrophils from skull bone marrow exert immunosuppressive and neuroprotective effects after TBI.颅骨骨髓中表达骨钙素的中性粒细胞在 TBI 后发挥免疫抑制和神经保护作用。
Cell Rep. 2024 Sep 24;43(9):114670. doi: 10.1016/j.celrep.2024.114670. Epub 2024 Aug 30.
3
Bioinformatics gene analysis for potential biomarkers and therapeutic targets of Parkinson's disease based on neutrophil extracellular traps.
基于中性粒细胞胞外诱捕网的帕金森病潜在生物标志物和治疗靶点的生物信息学基因分析
Front Aging Neurosci. 2024 May 31;16:1388226. doi: 10.3389/fnagi.2024.1388226. eCollection 2024.
4
Neutrophil Targeting Platform Reduces Neutrophil Extracellular Traps for Improved Traumatic Brain Injury and Stroke Theranostics.靶向中性粒细胞平台减少中性粒细胞胞外诱捕网,改善创伤性脑损伤和中风治疗学。
Adv Sci (Weinh). 2024 Jun;11(21):e2308719. doi: 10.1002/advs.202308719. Epub 2024 Mar 23.
5
Neutrophil extracellular trap-mediated impairment of meningeal lymphatic drainage exacerbates secondary hydrocephalus after intraventricular hemorrhage.中性粒细胞胞外诱捕网介导的脑膜淋巴管引流障碍加重脑室出血后继发性脑积水。
Theranostics. 2024 Feb 24;14(5):1909-1938. doi: 10.7150/thno.91653. eCollection 2024.
6
Potential Role of Bmal1 in Lipopolysaccharide-Induced Depression-Like Behavior and its Associated "Inflammatory Storm".Bmal1 在脂多糖诱导的抑郁样行为及其相关“炎症风暴”中的潜在作用
J Neuroimmune Pharmacol. 2024 Feb 2;19(1):4. doi: 10.1007/s11481-024-10103-3.
7
Neutrophils and Neutrophil Extracellular Traps Cause Vascular Occlusion and Delayed Cerebral Ischemia After Subarachnoid Hemorrhage in Mice.中性粒细胞和中性粒细胞胞外诱捕网导致小鼠蛛网膜下腔出血后血管闭塞和迟发性脑缺血。
Arterioscler Thromb Vasc Biol. 2024 Mar;44(3):635-652. doi: 10.1161/ATVBAHA.123.320224. Epub 2024 Feb 1.
8
Astrocyte-Derived Extracellular Vesicular miR-143-3p Dampens Autophagic Degradation of Endothelial Adhesion Molecules and Promotes Neutrophil Transendothelial Migration after Acute Brain Injury.星形胶质细胞衍生的细胞外囊泡 miR-143-3p 抑制急性脑损伤后内皮细胞黏附分子的自噬降解并促进中性粒细胞跨内皮迁移。
Adv Sci (Weinh). 2024 Feb;11(5):e2305339. doi: 10.1002/advs.202305339. Epub 2023 Dec 3.
9
Astrocyte KDM4A mediates chemokines and drives neutrophil infiltration to aggravate cerebral ischemia and reperfusion injury.星形胶质细胞 KDM4A 介导趋化因子并驱动中性粒细胞浸润,加重脑缺血再灌注损伤。
J Cereb Blood Flow Metab. 2024 Apr;44(4):491-507. doi: 10.1177/0271678X231216158. Epub 2023 Nov 26.
10
Correlation between Neutrophil-to-Lymphocyte Ratio and Cerebral Edema in Children with Severe Diabetic Ketoacidosis.重度糖尿病酮症酸中毒患儿中性粒细胞与淋巴细胞比值与脑水肿的相关性
Biomedicines. 2023 Nov 5;11(11):2976. doi: 10.3390/biomedicines11112976.